Probing the intracellular calcium sensitivity of transmitter release during synaptic facilitation
Probing the intracellular calcium sensitivity of transmitter release during synaptic facilitation
复制标题
DOI：
10.1016/s0896-6273(03)00085-0
复制
发表时间：
2003-03-06
期刊：
影响因子：
16.2
通讯作者：
Schneggenburger, R
中科院分区：
文献类型：
--
作者：
Felmy, F;Neher, E;Schneggenburger, R
在神经末梢，先前活动中残留的钙离子可以通过一种仍在争论的机制促进递质的释放。在这里，我们表明，细胞内钙敏感性的递质释放在保持在促进过程中很大程度上没有变化，这留下了一个微域钙信号增加作为一个可能的促进机制。我们测量了促进以及递质释放的钙依赖关系，以估计微域钙所需的增量。这些测量表明，残余和微域钙离子的线性总和仅占观察到的易化作用的30%。然而，细胞内钙信号总和的一小部分超线性，可能是由胞浆钙缓冲液(S)饱和引起的，足以解释该中枢神经系统突触的易化。
In nerve terminals, residual Ca2+ remaining from previous activity can cause facilitation of transmitter release by a mechanism that is still under debate. Here we show that the intracellular Ca2+ sensitivity of transmitter release at the calyx of Held is largely unchanged during facilitation, which leaves an increased microdomain Ca2+ signal as a possible mechanism for facilitation. We measured the Ca2+ dependencies of facilitation, as well as of transmitter release, to estimate the required increment in microdomain Ca2+. These measurements show that linear summation of residual and microdomain Ca2+ accounts for only 30% of the observed facilitation. However, a small degree of supra-linearity in the summation of intracellular Ca2+ signals, which might be caused by saturation of cytosolic Ca2+ buffer(s), is sufficient to explain facilitation at this CNS synapse.